Käytösoireisen muistisairaan lääkkeettömät hoitotyön keinot : Opas sairaanhoitajille

Aiheena opinnäytetyölle oli Käytösoireisen muistisairaan lääkkeettömät hoitotyön keinot – opas sairaanhoitajille. Opinnäytetyön tavoitteena oli tuottaa tietoa muistisairaan käytöshäiriöiden syistä ja lisäksi lisätä ymmärrystä sairaanhoitajille muistisairaan haasteellisen käytöksen lisääntymisestä. Opinnäytetyön tarkoituksena oli tuottaa yhteistyökumppanille opas, joka sisältää yleisimmät muistisairaudet ja niihin liittyvien käytöshäiriöiden ilmenemismuodot aiheuttajineen ja vaikuttavine tekijöineen. Tämän lisäksi opas sisältää hoitotyön keinoja, joiden avulla sairaanhoitaja pystyy havainnoimaan ja lieventämään muistisairaan käytösoireita. Opinnäytetyö on tehty yhteistyössä Suupohjan peruspalveluliikelaitoskuntayhtymän hoidon ja hoivan alueen kanssa. Etenevien muistisairauksien diagnostiikkaan kuuluu käytösoireiden lisääntyminen. Käytösoireita on muistisairauksien kaikissa vaiheissa ja niiden ilmaantuminen voi johtaa liialliseen ja turhaan rauhoittavien lääkkeiden määräämiseen ja käyttöön, on kuitenkin hyvä huomioida kokonaisvaltainen hoito, joka on potilaan yksilöllisen tilanteen huomioon ottava. Muistisairaiden määrä kasvaa nopeasti, varhaisen diagnosoinnin avulla pystytään ylläpitämään sairastuneen toimintakykyä ja huomioimaan sairastuneen oman elämänlaadun pysyminen hyvänä, unohtamatta hänen läheisiään. Käytösoireisen potilaan hoitolinja tulisi valita arvioimalla oireita ja selvittämällä niiden syy. Lääkkeettömän hoidon tarkoitus on, että muistisairaasta huolehditaan kokonaisvaltaisesti ja mahdollisimman hyvin hänen tarpeensa huomioon ottaen. Sairastuneen toimintakyvyn tukeminen on tärkeää, silloin hän tuntee olonsa turvatuksi ja arvostetuksi. Hyvien elämäntapojen huomioiminen, riittävän unen ja aktiviteetin turvaaminen tukevat sairastuneen tasapainon tunnetta. Käytöshäiriöiden syntyyn vaikuttaa myös ympäristössä tapahtuvat muutokset. Sairaanhoitajan on tärkeä luoda sairastuneelle tässä tilanteessa rauhallinen ja turvattu ympäristö.The subject for the thesis is non-drug nursing methods of a patient with memory disease and behavioural disorder. The aim of the thesis was to provide information on the causes of behavioural disorders of a patient with memory disease, and in addition, to increase nurses’ understanding about the negative behaviour of memory patients. The purpose of the thesis was to produce a guide containing the most common memory disorders and related manifestations of behavioural disorders, with their causes and contributing factors. In addition, the guide includes nursing tools that help the nurse to observe and mitigate the behavioural disorders of a patient with a memory disease. The thesis has been carried out in cooperation with the treatment and care area of The Suupohja Area Health and Social Services Joint Municipal Board. The diagnostics for progressive memory diseases include an increase in behavioural disorders. There are behavioural disorders at all stages of memory disorders, and their appearance may lead to the prescription and use of excessive and unnecessary medication. However, it is good to take into account the holistic treatment that is appropriate to the patient's individual condition. The number of patients with memory disease is increasing rapidly. With early diagnosis, it is pos-sible to maintain patients’ functional ability and take account of their quality of life, not forgetting their close relatives. The treatment line for the patient with behavioural disorder should be selected by evaluating the symptoms and finding out their cause. The purpose of non-drug nursing is that the patient with memory disorder is taken care of comprehensively, and his or her needs are taken into account as well as possible. Supporting the functional ability of the patient is important, and he or she feels secure and appreciated. Paying attention to a good lifestyle, ensuring adequate sleep and activity support the balance feeling of the patient. Changes in the environment also affect the appearance of behavioural disorders. It is important for the nurse to create a calm and secure environment for the patient in this situation

Chromosomal locations of human <i>ZBED</i> genes, frog <i>ZBEDX</i> and human Buster1 (<i>ZBED5</i>).

a<p>Positions in the human genome (hg19 assembly), and the frog genome (<i>Xenopus tropicalis</i>, xenTro3 assembly).</p>b<p>Also referred to in the literature as hDREF, Tramp, and Human-<i>Ac</i>.</p>c<p>The frog <i>ZBEDX</i> gene.</p>d<p>This gene is also referred to as Buster1 of the <i>Buster</i> DNA transposon family in the literature, and is distinct from other ZBEDs.</p>e<p>Sequence conversion is not currently available for these genomes in the UCSC Genome Browser (<a href="http://genome.ucsc.edu" target="_blank">http://genome.ucsc.edu</a>).</p

Phylogenetic relationships of separate BED domains.

<p>Roman numerals refer to BED domain position within ZBED genes (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0059940#pone-0059940-g001" target="_blank">Fig. 1</a>). Grey boxes on branches indicate hypothesized BED domain duplication events for the various <i>ZBED</i> genes. Posterior probabilities are provided next to tree nodes.</p

ZBED evolution.

<p>Phylogenetic tree for <i>ZBED</i> genes and related sequences from the <i>Ac</i> family. Two separate ZBED domestications are indicated. Numbers of included taxa are provided next to schematic clades. Active DNA transposons are marked with asterisks, and bold branches indicate posterior probabilities ≥95%.</p

Phylogenetic relationships of Buster1 (ZBED5).

<p>ZBED5 is identical to Buster1 and groups within the <i>Buster</i> family with strong support. Buster sequences are separate from collapsed clades representing the <i>Ac</i> family. Active DNA transposons are marked with asterisks, and bold branches indicate posterior probabilities ≥95%. Proposed nomenclature updates for ZBEDs 7, 8 and 9 are indicated next to branches ancestral to the respective ZBED (Buster) clade.</p

Endocranial associated dura mater blood vessels and Icam1 positive cells.

<p><b>A)</b> Representative immunohistochemical staining (brown) for platelet/endothelial cell adhesion molecule 1 (Pecam1) positive blood vessels in decalcified calvaria sections. Arrowheads indicate small and flat Pecam1 positive blood vessel present in the dura mater membrane (covering the endocranial bone surface) of control tissue. In the “Vitamin A” panel the Pecam1 positive blood vessels are readily visible and appear engorged. Asterisks indicate osteoclasts in close proximity to the enlarged vessels, a combination only found in vitamin A animals. e = endocranial bone surface <b>B)</b> Immunohistochemical staining (brown) for intercellular adhesion molecule 1 (Icam1) in decalcified calvaria sections. Brackets indicate position of the dura mater membrane which is highly Icam1 positive only in vitamin A animals. Asterisks indicate osteoclasts in close proximity to the Icam1 positive cells, only found in vitamin A animals. Right panel shows the number of Icam1 positive cells/section in the dura mater (n = 4 and 6 sections/group and each group contain sections from 3 different individuals). Results are given as means + SD. ** p < 0.01.</p

Osteocyte phenotype and RA-induced gene expression in osteoblastic cells.

<p><b>A)</b> Representative picture of TRAP-stained decalcified bone section from mice fed excessive doses of vitamin A and controls. White arrowheads show TRAP-positive osteocytes close to the osteoclast rich endocranial surface and black arrowheads show TRAP-negative osteocytes. The asterisk indicates osteoclast attached to bone. <b>B)</b> Left panel shows a representative picture of Trichrome stained decalcified bone sections. Inset black box shows magnified osteocytes used for measurement of perilacunar matrix area (blue stain). The asterisks indicate osteoclasts. The right panel shows osteocyte perilacunar matrix area measured as number of blue pixels, analyzed from pictures of Trichrome stained bone sections (n = 10 osteocytes/group and each group contain sections from 3 different individuals). <b>C)</b> Osteoblastic (MC3T3-E1) gene expression after 24h of 400 nM retinoic acid (RA) treatment as determined by quantitative RT-PCR analysis. Runx2 (runt related transcription factor 2), Sp7 (Sp7 transcription factor 7, osterix), Dmp1 (dentin matrix protein 1), Tnfsf11 (tumor necrosis factor ligand superfamily member 11, RANKL), Acp5 (acid phosphatase 5, tartrate resistant, TRAP), Ctsk (cathepsin K), Mmp9 (matrix metalloproteinase 9) and Mmp13 (matrix metalloproteinase 13). <b>D)</b> Mature osteoblastic/osteocytic (differentiated MC3T3-E1 cells) gene expression after 24h of 400 nM retinoic acid (RA) treatment as determined by quantitative RT-PCR analysis. Bglap2 (bone gamma-carboxyglutamate protein 2, osteocalcin), Ibsp (integrin binding sialoprotein) and as described in (C). <b>E)</b> Primary mouse calvaria osteoblast gene expression after 24h of 400 nM retinoic acid (RA) treatment as determined by quantitative RT-PCR analysis. Results are given as means + SD. * p < 0.05, ** p < 0.01 and *** p < 0.001.</p

RA and RAR-dependent effects on osteoblast proliferation and on treatment start during <i>in vitro</i> mineralization.

<p>(<b>A</b>) Cell proliferation of MC3T3-E1 cells, treated with 400 nM RA or 1 µM AGN during the first 14 days of a mineralization experiment. (<b>B</b>) Cell number of viable and non-viable MC3T3-E1 cells after 10 days, with or without 400 nM RA. (<b>C</b>) Alizarin Red stain quantification of MC3T3-E1 cells, treated with 400 nM RA or 1 µM AGN from day 0, 10, 14 or 18 followed by analysis at day 25. Control mineralization level is set at 1 and dotted line represent background (no osteogenic induction). Means +/– SD, * p<0.05, ** p<0.01 and *** p<0.001 vs Control.</p

The calvarial bone and osteoblast phenotype.

<p><b>A)</b> Illustration of peri- (peri), endo- (endo) and intra- (intra) cranial bone surfaces. <b>B)</b> Left panel: μCT picture of a pericranial and a dorsal view of isolated skull bones from mice fed excessive doses of vitamin A and control mice. F = frontal, P = parietal, Ip = Interparietal and Oc = occipital. Right panel are high power pictures of boxed areas in left panel, and show the intersection of the coronal (arrowheads) and sagittal (asterisk) sutures. <b>C)</b> Left panel: representative μCT pictures of transverse sections at the mid parietal bone (sagittal suture, arrow). Right panel: high power pictures of boxed area in the left panel. Arrowheads highlight the rougher endocranial surface in calvarial bone from vitamin A mice. <b>D)</b> Histomorphometric analyses of transverse bone area and mineralized area (n = 4/group). <b>E)</b> Left panel: pictures showing calcein double labelling of pericranial surface. Right panel: dynamic histomorphometric results, from analysis of the calcein double labeling. Pericranial mineral apposition rate (Peri. MAR) and pericranial bone formation rate (Peri. BFR) (n = 4/group). Results are given as means + SD. * p < 0.05.</p

QRT-PCR analysis of genes associated with osteoblast differentiation and endogenous RA degradation.

<p>(<b>A</b>) Expression levels of mRNA for <i>Alpl (alkaline phosphatase, liver/bone/kidney)</i> and <i>Bglap</i> (<i>Osteocalcin)</i> during a mineralization experiment of MC3T3-E1 cells treated with 400 nM RA or 1 µM AGN. (<b>B</b>) mRNA expression of <i>Cyp26b1</i> at day 1, treated as in (A). (<b>C</b>) mRNA expression of <i>Cyp26b1</i> at day 1, 3, 7, 14 and 21 of a mineralization experiment of MC3T3-E1 cells +/– 1 µM AGN. Means +/– SD, * p<0.05, ** p<0.01 and *** p<0.001 RA vs Control. # p<0.05, ## p<0.01 and ### p<0.001 AGN vs Control. ¤ p<0.05 and ¤¤¤ p<0.001 vs Control day 1.</p